UMEM Educational Pearls

Drug-Induced Thrombocytopenia

• Thrombocytopenia is common in critically ill patients and is associated with increased mortality.
• Up to 25% of critically ill patients will develop thrombocytopenia as a result of a medication, termed drug-induced thrombocytopenia (DIT)
• Antibiotcs are a common, yet infrequently recognized, cause of DIT.
• Antibiotics reported to cause DIT include linezolid, vancomycin, trimethoprim/sulfamethoxazole, and the beta-lactams.
• In fact, piperacillin/tazobactam has been associated with DIT more frequently than any other penicillin. 

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Classic electrocardiographic findings for hypokalemia:
u-waves (produces appearance of long QT), especially in the precordial leads
ventricular ectopy (PVCs typically)
ST segment depression or downward sagging, especially in the precordial leads

note that the sagging ST segments that terminate in large U-waves end up producing biphasic T-waves; these have the mirror image appearance of Wellens waves

• Back pain is the most common musculoskeletal complaint that results in visits to the ED.
• It has a benign course in more than 90% of patients, so we must be vigilant and comfortable looking for warning signs of a neurologically impairing or life-threatening cause.
• We rely on the presence of so-called "red flags" or alarm symptoms to guide further diagnostic tests, specialty evaluation, and treatment. 
• Additionally, always consider 2 important extra-spinal causes of back pain: aortic dissection (sudden onset back pain) and abdominal aortic aneurysm (patients >50, esp. those who you think have a kidney stone- isolated back and groin pain is a common presentation).

A patient arrives via EMS agitated with VS: P 140, BP 155/100, R 18, T 101F. There is an admitted drug exposure and you examine his eyes which are dilated. You shine the light in the eyes - if the pupil reacts, would that be consistent with anticholinergic or sympathomimetic toxidrome?

Answer: Anticholinergic exposure paralyzes pupillary constrictor muscles and causes dilated pupils that do not react to light. Think about when you go to the eye doctor's office. They put homoatropine in your eyes so that when they look with the slit lamp they can see the retina without interference from pupillary constriction. Sympathomimetic exposure like cocaine activates pupillary dilator muscles, the constrictors are still intact and will give a reflexive constriction to light.  This patient has reactive pupils and by the mere fact is in Baltimore probability dictates a sympathomimetic exposure like cocaine.

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• Several medications such as dopamine-blocking anti-emetics, triptans, and ergotamine derivatives have been shown to more effectively treat migraine headaches over other types of headaches, making the ability to accurately recognize this common (2.2% of all ED visits) condition essential.

• According to the International Headache Society, one meets diagnostic criteria for migraine headache without aura when they have experienced at least 5 attacks, each lasting 4 to 72 hours (untreated or unsuccessfully treated) and accompanied by at least 2 of the 4 following characteristics ("PUMA"):

          A.

              1.  Pulsatile or throbbing in quality

              2.  Unilateral in location

              3.  Moderate to severe in intensity

              4.  Aggravated by activity (i.e.climbing stairs, exertion), plus

         B.  at least 1 of the following 2 during the headache  ("VP"): 

              1.  Vomiting and/or nausea

              2.  Photophobia and/or phonophobia

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ICU Acquired Weakness

• ICU acquired weakness (ICU-aw) is a general term that refers to the weakness that develops in critically ill patients during the course of their illness - especially in patients with sepsis and those receiving mechanical ventilation.
• ICU-aw is an very common complication of critical illness that can develop within hours and has been shown to increase the duration of mechanical ventilation and ICU/hospital LOS.  Observational studies have also reported an association with mortality.
• Risk factors associated with ICU-aw include medications (neuromuscular blocking agents, corticosteroids), hyperglycemia and immobility.
• For the critically ill ED patient, current recommendations suggest limiting the administration of neuromuscular blocking agents and corticosteroids, when possible.

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There are multiple reasons for ST-segment elevation, the most important of which is acute myocardial infarction. However, because the treatment difference between MI vs. other more benign causes is so important, one should keep in mind the following factors that strongly point toward the diagnosis of MI:
1. the presence of ST-segment depression in any lead aside from aVR or V1
2. ST elevation that is horizontal or convex upwards (like a tombstone)
3. ST or T-wave morphologies that change over time with serial testing
4. ST changes compared to old ECGs
5. the development of Q-waves
6. ST elevation that follows coronary anatomy (e.g. limited to inferior leads, anterior leads, or lateral leads)

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The Salter Harris  Classification System is used in pediatric epiphyseal fractures.  The higher the type of fracture the poorer the prognosis

Some common exam facts about Salter Harris Fractures are:

1. The type II fracture is the most common.
2. The small metaphyseal fragment in Salter Harris type II and IV fractures is called the Thurston Holland Sign.
3. Type III and IV fractures often require open reduction and internal fracture due to the fracture extending into the joint.
4. Type V fractures may appear normal, but the epiphyseal plate is crushed and the blood supply is interrupted.

The Classification system as listed by Type:

• Type I: A fracture through the physeal growth plate. Typically can not be seen on x-ray unless they growth plate is widened.
• Type II: A fracture through the physeal growth plate and metaphysis.
• Type III: A fracture through the physeal growth plate and epiphysis.
• Type IV: A fracture through the physis, physeal growth plate and metaphysis.
• Type V: A crush injury of the physeal growth plate.

A image of the fractures can be found on FP Notebook at http://www.fpnotebook.com/_media/OrthoFractureSalterHarris.jpg

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Valproic Acid (Depakote) is a drug that uniquely has the ability to raise serum ammonia concentrations. It is able to do this without raising liver er enzymes and it can occur in overdose or at therapeutic levels. Do not think of this in the context of hepatic encephalopathy. This a metabolic derangement caused by VPA.

• Any patient with somnolence, lethargy, decreased responsiveness - order a serum ammonia level as well as Valproic acid level
• If the serum ammonia is elevated in conjunction with altered mental status consider a trial of carnitine
• L-carnitine is a safe drug that is used in nutritional supplementation. VPA and other anticonvulsants cause carnitine deficiency
• Most effective dose is unknown but from a recent review: IV 100 mg/kg once, followed by infusions of 50 mg/kg (to a maximum of 3 g per dose) every 8 hours until patient improves, ammonia decreases

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  Perrott J, Murphy NG, Zed PJ. L-carnitine for acute valproic Acid overdose: a   systematic review of published cases. Ann Pharmacother. 2010  Jul-Aug;44(7-8):1287-93. Epub 2010 Jun 29.

• Lacunar infarcts affect the deep penetrating vessels of the middle cerebral artery and carry the best prognosis of all strokes.

• There are 4 classic syndromes characteristically caused by lacunar infarcts, with which the emergency physician should be familiar and able to recognize.  They are:

1. Pure motor hemiparesis.
2. Pure sensory syndrome.
3. Ataxic hemiparesis (ipsilateral cerebellar and motor symptoms).
4. Clumsy hand dysarthria syndrome (ipsilateral hand weakness, patient may say their hand "feels awkward," dysarthria more pronounced than the weakness).

Drug-Drug Interactions in the Critically Ill

• Critically Ill ED patients are at risk for drug-drug interactions (DDIs) due to altered organ function, polypharmacy, and altered drug kinetics.
• DDIs involving the cytochrome isoenzyme CYP3A4 are of particular importance.
• CYP3A4 inhibitors, such as macrolides and azoles (fluconazole, voriconazole), can cause serious DDIs when given concomitantly with meds that are a subtrate for CYP3A4 - midazolam, cyclosporine, tacrolimus, diltiazem, amiodarone.
• Pay particular attention to your transplant patients, as administration of an azole can result in significant cyclosporine or tacrolimus toxicity.

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Pneumoperitoneum on CXR and CT

Pneumoperitoneum may be seen on an upright CXR up to 7 days after laparoscopic abdominal surgery/laparotomy and may be seen on abdominal CT for as long as three weeks after surgery. 

Elderly patients are at higher risk for skin infections for numerous reasons:
1. Blunted immune system response of skin to infections.
2. Slower wound repair after 3rd decade.
3. More frequent exposure to infections, especially drug resistant infections, especially if the patient is frequently hospitalized or in nursing homes.
4. Frequent portals of entry for skin infections: indwelling tubes and lines, leg ulcers, fissures and maceration on feet and between toes.

A key takeaway point is to always check the skin thoroughly of your elderly patients when searching for infections, especially the feet and toes!

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• Spondylolysis is a unilateral or bilateral defect in the pars interarticularis portion of the vertebrae.
• It is a stress fracture mostly seen in the lumbar vertebrae, and most commonly L5.
• Pain is relieved with rest and worsened by lateral bending or extension (NOTE: most back pain is worsened by flexion).
• If neurologic symptoms and/or radiculopathy are present, an alternative diagnosis should be considered, because they are rarely associated with spondylolysis.
• Diagnostic imaging should start with plain radiographs with added oblique views.
• Classically, oblique views show the Scotty dog sign with a crack on the dog’s neck/collar, the pars.

http://www.gentili.net/signs/images/400/spinescottyparsdefectdrawing.JPG

The Scotty dog’s head (superior articular facet), nose (transverse process), eye (pedicle), neck (pars interarticularis), and body (lamina) should be easily identified on the oblique radiograph.
 

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In a patient with toxin-induced bradycardia and hypotension, here is a quick differential to help identify the responsible substance:

• Beta blockers
• Calcium channel blockers
• Cholinergics
• Clonidine (and other alpha-2 agonists)
• Digoxin (and other cardiac glycosides)
• Opioids
• Sedative hypnotics (such as benzodiazepines and barbiturates)

Less commonly seen causes include: magnesium, propafenone, and plant toxins (aconitine, andromedotoxin, veratrine).

• The ability to detect brain CT abnormalities suggestive of ischemic stroke largely depends upon the time between the onset of symptoms and the CT examination.

• Large, cortical strokes are typically not detected on CT for at least 3 hours; Nearly 60% of strokes, however, are detectable on CT within 24 hours from time of infarct, and essentially 100% within 7 days.

• Clinical correlation:  Be sure that the reported time of symptom onset properly correlates with brain CT findings, as this could affect the decision to treat with tPA in accordance with appropriate time windows.  If a patient reports 1 hour of stroke symptoms, for example, and the brain CT shows significant edema and loss of gray/white matter differentiation suggesting infarct, be wary of a time discrepancy.

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Asthma, Peak Pressures, and the Ventilator

• In previous pearls, we have highlighted ventilator settings for the asthmatic, along with the differences between peak and plateau pressure measurements.
• When ventilating the asthmatic, pay attention to the ventilator settings placed by your respiratory therapist.
• In general, the respiratory therapist will set the ventilator to stop delivering tidal volumes when the peak pressure exceeds 40-60 cm H₂O.
• For asthmatics, this practice can result in very low tidal volumes.
• Thus, peak pressure limits must be set higher.
• As you know, high peak pressures have not been shown to be injurious, provided that the plateau pressure remains < 30 cm H₂O

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Risk Stratification in Pulmonary Embolism

The following are the principal markers useful for risk stratification:

• Clinical markers (shock, hypotension)
• Markers of RV dysfunction (RV dilatation, hypokinesis or pressure overload on echo, RV dilatation on CT, BNP elevation)
• Markers of myocardial injury (elevated troponin)

Patients with one or more of these markers have a higher mortality rate.

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The majority of "classic" symptoms and signs in elderly patients with pneumonia (fever, cough, sputum production, leukocytosis,chest pain) are unreliably present. However, tachypnea is one of the most reliable early findings in elderly patients with pneumonia, and in fact the same can be said about other serious bacterial illnesses in the elderly. The takeaway point here is simple: always count the respiratory rate in elderly patients (and don't trust those triage respiratory rates)!

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Diverticular Bleeding

• Diverticular bleeding is the  most common source of lower GI bleeds and accounts for 17 to 40 percent of cases
• The most common presentation (80%) is massive painless rectal bleeding. 
• Patients may have some cramping prior to a bloody bowel movement but otherwise will typically have no abdominal pain.
• The majority of the cases will resolve spontaneously, but those requiring more than 4 units of Packed Red Blood Cells should be considered for an angiogram or  surgery.
• Angiography can be used to localize the site of bleeding and embolize the bleeding source. 
• If embolization fails the patient may require a partial colectomy to treat the bleeding source.

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